The eyes are the window to the brain: reviewing oculomotor abnormalities in obsessive-compulsive disorder

In this issue of Acta Psychiatrica Scandinavica, Jaafari et al. (1) have reviewed the literature examining eye-movement abnormalities in obsessive-compulsive disorder (OCD). In so doing, they have collected data from disparate sources, including studies in which OCD subjects were used in secondary analyses making these studies harder to identify in the literature. The authors report that in OCD, smooth pursuit movements are mildly impaired, and that OCD is associated with longer latencies on antisaccade tasks. However, these deficits were determined to be subtle, and performance on these measures did not correlate with symptom severity. These findings are in contrast to schizophrenia, in which eye movements are consistently and profoundly impaired.

Eye movements are coordinated by frontocortical-basal ganglia loop circuits that anatomically overlap with other basal ganglia loop circuits modulating movement, cognition, and affect (2). Given that many of the same basal ganglia circuits implicated in schizophrenia are also implicated in OCD, the extent to which simple eye movement tasks can distinguish these patients from those with schizophrenia is striking. As the authors point out, this could be because of the distinct contributions of the dorsolateral prefrontal cortex in schizophrenia and the orbitofrontal cortex in OCD. More broadly speaking, it also implies that non-invasive oculomotor measures may be able to provide us with highly selective functional information that maps onto discrete anatomical circuits. Alternatively, the evidence discussed by Jaafari et al. suggests that the very same circuits may be important to both OCD and schizophrenia, but dysfunctional under different conditions, with complex cognitive tasks showing preferential impairment in OCD. Thus, eye movement measures may provide us with a way of monitoring the flow of information through shared areas of vulnerability that may be differentially disrupted depending on task demands and/or etiological factors.

Mental illnesses are presently defined categorically by symptom-based checklists. Increasingly, shortcomings in this approach have been recognized. For example, symptoms commonly span multiple diagnostic boundaries and heterogeneity is pervasive, making few patients encountered in clinical practice ‘typical’. These factors greatly limit the extent to which treatment outcomes or illness progression can be predicted. Moreover, modern neuroscience, genetics, and neuropsychology all agree that the current categorical systems do not ‘carve nature at the joints’, creating both false dichotomies and spurious associations in nomenclature that are unsupported by biological mechanisms. In trying to modernize, efforts to redefine mental illness in terms of objective dimensions of biological processes have been initiated (3).

Of interest to the present work by Jaafari et al., one of the disorders most amenable to this neuro-circuitry-based approach to classification is OCD, and the associated spectrum of tic disorders, anorexia nervosa, and others. As neuroimaging studies have strongly implicated cortical-basal ganglia loop circuits in the pathology of OCD, there is already a well-defined anatomical pathway of interest. However, clinical features across the OCD spectrum differ, and as mentioned, the basal ganglia loop circuits impact upon clinically distinct psychiatric disorders such as schizophrenia. Thus, while these pathways are of particular interest to OCD, the ways in which they are common and unique across disorders remains unclear and requires elaboration.

While, the research reviewed by Jaafari et al. is not particularly novel, the recent emphasis on brain-based approaches to diagnosis suggests that this literature should be carefully re-examined with an eye toward establishing biological markers that could assist in mechanism-based categories of psychiatric illnesses. While Jaafari et al. conclude that eye movement measures have little current value in diagnosing OCD, it is worth noting, that in many cases the studies reviewed showed conflicting results, or that some subgroups were noticeably affected. Perhaps these are the very subjects that a biologically based assay could identify more reliably than a categorically based OCD diagnosis.

Regardless of the specific technology, psychiatry must prepare for the inevitable arrival of conceptual and technical change. The diagnostic principles of tomorrow will almost certainly require expertise outside the bounds of training presently conferred to most psychiatrists. If psychiatry does not keep pace, it risks ceding ground to other specialties with more established traditions in technological advance. One need only look to epilepsy and dementia to see that once a mechanistic explanation of a disorder is developed, it invariably changes from a ‘functional’ to an ‘organic’ illness, and risks moving out of the domain of psychiatry. If clinical neuroscience is perceived as ‘too hard’ for psychiatrists, we will lose our patients to other specialties and face hard questions about our roles in medicine. The review by Jaafari et al. is a good reminder that we need to approach these issues broadly with an open mind for innovation.